Genetic control of cytolytic t-lymphocyte responses. II. The role of the host genotype in parental leads to F1 radiation chimeras in the control of the specificity of cytolytic T-lymphocyte responses to trinitrophenyl-modified syngeneic cells.
01 Aug 1978-Journal of Experimental Medicine (The Rockefeller University Press)-Vol. 148, Iss: 2, pp 352-359
TL;DR: It is demonstrated that the host environment where T cells differentiate influences the specificity of the primary cytolytic T-lymphocyte (CTL) response to TNP-modified syngeneic antigens.
Abstract: Bone marrow cells from C3H (H-2k) mice, a strain that does not exhibit cross-reactive lysis of trinitrophenyl (TNP)-modified allogeneic targets, were allowed to mature in heavily irradiated (B6 times C3H)F1 (H-2b/k) recipients, an F1 hybrid that does demonstrate cross-reactive lysis. Spleen cells from these chimeric mice were removed after 3-4 mo and by H-2 typing shown to be of C3H origin. These cells were found to be tolerant to B6 alloantigens by mixed lymphocyte reaction and cell-mediated cytotoxicity and, when stimulated in vitro with TNP-modified syngeneic cells, now cross-reactively lysed TNP-modified allogeneic targets. These studies demonstrate that the host environment where T cells differentiate influences the specificity of the primary cytolytic T-lymphocyte (CTL) response to TNP-modified syngeneic antigens.
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TL;DR: F 1 helper T cells which differentiate in a parental thymus graft show preference for B cells of that parent when tested in naive nude recipients, but parental T cells who differentiate in an F 1 or allogeneic thymos do not show any learning when tested under these conditions.
8 citations
01 Jan 1979
TL;DR: The various categories of infectious agents that confront higher vertebrate hosts are quite different with respect to acuteness and rapidity of the disease process they incite, so the evolutionary or selective pressure that ultimately determines whether the relationship between parasite and host becomes symbiotic or parasitic is also decisive in shaping a particular part of the host physiology specifically for that function.
Abstract: The various categories of infectious agents that confront higher vertebrate hosts are quite different with respect to acuteness and rapidity of the disease process they incite. Consequently, the evolutionary or selective pressure that ultimately determines whether the relationship between parasite and host becomes symbiotic or parasitic is also decisive in shaping a particular part of the host physiology specifically for that function. Since most parasites have an enormously faster generation cycle than the vertebrate host, the parasites’ adaptive capacity is much the greater of the two. The ultimate equilibrium of the host-parasite relationship and their relative capacity to adapt mutually are obviously determined by both parties. What establishes this balance is poorly understood, but, viewed teleologically, survival of both parasite and host seems to keep the relationship in check. Within the vertebrate host whose reactive systems are called into play by such infections, immune responses by antibodies and cells (reviewed in Notkins, 1975, Bloom and Rager-Zisman, 1975; Blanden et al., 1976b), nonspecific resistance by macrophages (Lindenmann et al., 1978; Cheers and McKenzie, 1978) or other cells, past and present experience with infection, as well as concurrent infections all play some part.
8 citations
01 Jan 1981
TL;DR: T-cell cytotoxicity against virus-infected or chemically modified target cells, or target cells expressing minor histocompatibility antigens, involves corecognition of the MHC D- or K-region products.
Abstract: Numerous recent studies in rodents have demonstrated that T-cell immune responses to antigen are restricted by products of the major histocompatibility complex (MHC) of the animal under study [for references, see Paul and Benacerraf (1977) and Thorsby (1978), as well as Chapters 1,3, and 8]. Available data may be summarized as follows:
1.
Macrophage-dependent antigen activation of T cells involves corecognition of antigen and products of the MHC immune-response (I) region.
2.
T-cell help for B-cell antibody production involves recognition of the MHC I-region products expressed in the B cells.
3.
T-cell cytotoxicity against virus-infected or chemically modified target cells, or target cells expressing minor histocompatibility antigens, involves corecognition of the MHC D- or K-region products.
5 citations
01 Jan 1980
TL;DR: The requirement that T cells recognize T-dependent antigens in relationship with self MHC gene products can explain Ir gene phenomena by two distinct mechanisms.
Abstract: Publisher Summary It is widely recognized that T cells, with the probable exception of suppressor cells, only recognize thymus-dependent antigens in association with autologous MHC gene products on the surface of cells and that macrophage presentation in conjunction with their la molecule is essential to initiate thymus-dependent immune responses. This chapter discusses (1) the commitment of T cells other than suppressor cells to the recognition of thymus-dependent antigens in relation to autologous MHC antigens and (2) the manner in which the la molecules, in the case of antigen presentation by macrophages and, in a parallel manner, the K and D products, in the case of CTL responses, contribute to the T cell specificity, thereby giving rise to the phenomenology of Ir gene control of immune responses. T cells initially specific for autologous MHC gene products are selected in the thymus to differentiate and proliferate. Then, in a second stage, only those T cells that bear low-affinity receptors for self MHC antigens are allowed to mature and leave the thymus as functional mature T cells. Such T cells, having low reactivity for autologous MHC antigens, have concommitently high affinity for the variants of self MHC antigens. The requirement that T cells recognize T-dependent antigens in relationship with self MHC gene products can explain Ir gene phenomena by two distinct mechanisms.
4 citations
01 Jan 1980
TL;DR: While some immune responses do not involve cell-mediated immunity mediated by thymus-derived (T) lymphocytes, most types of responses are at least indirectly dependent on the ability to activate antigen-specific T lymphocytes.
Abstract: Neoplastic cells express cell-surface antigenic molecules, referred to as tumor-associated transplantation antigens (TATA), that can be recognized by the host’s immune system (Gross, 1943; Foley, 1953; Prehn and Main, 1957). A consequence of such recognition is the production of either a humoral and/or a cell-mediated immune response which may or may not lead to protective immunity against the tumor (reviewed by Hellstrom and Hellstrom, 1969). While some immune responses do not involve cell-mediated immunity mediated by thymus-derived (T) lymphocytes, most types of responses are at least indirectly dependent on the ability to activate antigen-specific T lymphocytes.
2 citations